Molecular Basis of Cardioprotective Effect of Antioxidant Vitamins in Myocardial Infarction
Author
dc.contributor.author
Rodrigo Salinas, Ramón
Author
dc.contributor.author
Libuy, Matías
es_CL
Author
dc.contributor.author
Feliú, Felipe
es_CL
Author
dc.contributor.author
Hasson, Daniel
es_CL
Admission date
dc.date.accessioned
2014-01-30T14:51:31Z
Available date
dc.date.available
2014-01-30T14:51:31Z
Publication date
dc.date.issued
2013
Cita de ítem
dc.identifier.citation
BioMed Research International Volume 2013, Article ID 437613, 15 pages
en_US
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/129226
General note
dc.description
Artículo de publicación ISI
en_US
Abstract
dc.description.abstract
Acute myocardial infarction (AMI) is the leading cause of mortality worldwide.Major advances in the treatment of acute coronary
syndromes andmyocardial infarction, using cardiologic interventions, such as thrombolysis or percutaneous coronary angioplasty
(PCA) have improved the clinical outcome of patients. Nevertheless, as a consequence of these procedures, the ischemic zone is
reperfused, giving rise to a lethal reperfusion event accompanied by increased production of reactive oxygen species (oxidative
stress). These reactive species attack biomolecules such as lipids, DNA, and proteins enhancing the previously established tissue
damage, as well as triggering cell death pathways. Studies on animal models of AMI suggest that lethal reperfusion accounts for up
to 50% of the final size of a myocardial infarct, a part of the damage likely to be prevented. Although a number of strategies have
been aimed at to ameliorate lethal reperfusion injury, up to date the beneficial effects in clinical settings have been disappointing.
The use of antioxidant vitamins could be a suitable strategy with this purpose. In this review, we propose a systematic approach
to the molecular basis of the cardioprotective effect of antioxidant vitamins in myocardial ischemia-reperfusion injury that could
offer a novel therapeutic opportunity against this oxidative tissue damage.